Distribution of Polymorphisms of the Renin—Angiotensin System Genes (ACE, AGT, and AGTR1), ITGB3, and FTO in Pregnant Patients with Hypertensive Disorders

Zotova, T. Yu.; Lapaev, N. N.; Азова, М. М.; Благонравов, М. Л.; Gigani, O. O.; Aissa, A. Ait; Denisova, Anna P.

doi:10.1007/s10517-019-04464-6

Cited by 7 publications

(4 citation statements)

References 8 publications

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“… 54 Patients with gestation-associated arterial hypertension were showed to have higher incidence of heterozygotic genotype AT (FTO gene) than healthy puerperants. 55 These results reveal that m6A is closely related to hypertension, further study its epitranscriptomic mechanisms will provide us more concepts of the cause and treatment of hypertension.…”

Section: Hypertensionmentioning

confidence: 66%

The critical roles of m6A modification in metabolic abnormality and cardiovascular diseases

et al. 2021

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N6-methyladenosine (m6A) RNA methylation is an emerging area of epigenetics, which is a reversible and dynamic modification mediating by ‘writers’ (methylase, adding methyl groups, METTL3, METTL14, and WTAP), ‘erasers’ (demethylase, deleting methyl groups, FTO and ALKBH5), and ‘readers’ (YTHDF1-3, YTHDC1 and YTHDC2). Recent studies in human, animal models and cell levels have disclosed a critical role of m6A modification in regulating the homeostasis of metabolic processes and cardiovascular function. Evidence from these studies identify m6A as a candidate of biomarker and therapeutic target for metabolic abnormality and cardiovascular diseases (CVD). Comprehensive understanding of the complexity of m6A regulation in metabolic diseases and CVD will be helpful for us to understand the pathogenesis of CVD. In this review, we discuss the regulatory role of m6A in metabolic abnormality and CVD. We will emphasize the clinical relevance of m6A dysregulation in CVD.

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Section: Hypertensionmentioning

confidence: 66%

The critical roles of m6A modification in metabolic abnormality and cardiovascular diseases

et al. 2021

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“…A review study found that previous studies reported conflicting results, but the majority found that the DD genotype was associated with the incidence of hypertension and preeclampsia in pregnancy. A study of 121 pregnant women with a gestational age of 27–40 weeks reported a higher frequency of the DD genotype in the essential hypertension group than in the control group ( 21 ). A meta-analysis of 40 studies with a total of 3,977 cases and 7,065 controls concluded that the DD genotype increased the risk of preeclampsia compared with the DD and ID genotypes (52% vs. 17%), and D allele increased the risk of preeclampsia 1.29 times more than I allele ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

Association polymorphism of guanine nucleotide–binding protein β3 subunit (GNB3) C825T and insertion/deletion of the angiotensin-converting enzyme (ACE) gene with peripartum cardiomyopathy

Dewi

Wardhani

Maghfirah

et al. 2023

Front. Cardiovasc. Med.

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IntroductionPeripartum cardiomyopathy (PPCM) is a potentially life-threatening pregnancy-related heart disease. Genetic roles such as gene polymorphisms may relate to the etiology of PPCM. This study analyzes the association between single nucleotide gene polymorphism (SNP) guanine nucleotide–binding protein beta-3 subunit (GNB3) C825T and insertion/deletion (I/D) of the angiotensin-converting enzyme (ACE) gene with the incidence of PPCM.MethodsAn analytic observational study with a case–control design was conducted at the Integrated Cardiac Service Center of Dr. Soetomo General Hospital, Surabaya, Indonesia. PPCM patients of the case and control groups were enrolled. Baseline characteristic data were collected and blood samples were analyzed for SNP in the GNB3 C825T gene and for I/D in the ACE gene by using the polymerase chain reaction, restriction fragment length polymorphism, and Sanger sequencing. We also assessed ACE levels among different ACE genotypes using a sandwich-ELISA test.ResultsA total of 100 patients were included in this study, with 34 PPCM cases and 66 controls. There were significant differences in GNB3 TT and TC genotypes in the case group compared with that in the control group (TT: 35.3% vs. 10.6%, p = 0.003; TC: 41.2% vs. 62.5%, p = 0.022). The TT genotype increased the risk of PPCM by 4.6-fold. There was also a significant difference in the ACE DD genotype in the case group compared with that in the control group (26.5% vs. 9.1%, p = 0.021). DD genotypes increased the risk of PPCM by 3.6-fold. ACE levels were significantly higher in the DD genotype group than in the ID and II genotype groups (4,356.88 ± 232.44 pg/mL vs. 3,980.91 ± 77.79 pg/mL vs. 3,679.94 ± 325.77 pg/mL, p < 0.001).ConclusionThe TT genotype of GNB3 and the DD genotype of the ACE are likely to increase the risk of PPCM. Therefore, these polymorphisms may be predisposing risk factors for PPCM incidence. ACE levels were significantly higher in the DD genotype group, which certainly had clinical implications for the management of PPCM patients in the administration of ACE inhibitors as one of the therapy options.

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“…In vitro , FTO efficiently eliminated the m6A modification of mRNA ( 56 ). Recently, some studies have found strong associations between FTO and hypertension ( 57 ), diabetes ( 58 , 59 ), obesity ( 60 , 61 ), non-alcoholic fatty liver disease ( 62 , 63 ), atherosclerosis ( 64 ), myocardial infarction ( 38 , 65 ), ischemic reperfusion injury ( 65 ), cardiac hypertrophy ( 65 ), and heart failure ( 65 ). Thus, FTO considerably contributes to the progression of cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 99%

Modification of m6A mediates tissue immune microenvironment in calcific aortic valve disease

Chen¹,

Xiong²,

Sun³

et al. 2022

Ann Transl Med

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Background: Several human diseases are associated with aberrant expression of regulators involved in N6methyladenosine (m6A) RNA modification. However, their role in aortic valve calcification (AVC) is largely unknown. The aim of this study was to determine the general expression pattern and potential function of m6A regulators in AVC by bioinformatics methods. Methods:We obtained AVC datasets from the Gene Expression Omnibus (GEO). The identification of m6Arelated differentially expressed genes (DEGs) and the Consensus Clustering method was performed to type AVC individuals based DEGs. Then, we quantified the effect of typing by principal component analysis (PCA). Next, we performed the weighted gene co-expression network analysis (WGCNA) and identified the main modules as well as functional analysis. Additionally, the key genes were screened by protein-protein interaction network (PPIN) analysis and identifying important genes of important modules. We again typed AVC individuals by the same method using key genes. Finally, we evaluated the link between key genes and immune infiltration.Results: We discovered that METTL14, ZC3H13, FTO, FMR1, HNRNPA2B1, HNRNPC, LRPPRC, YTHDC1, YTHDC2, and YTHDF1 expression levels decreased considerably in AVC tissues. Based on 10 genes, we typed 240 AVC samples as clusters A and B. We assessed the immune cell content in 240 samples using Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT) and found that B cell memory, CD8 T cells, T follicular helper cells, monocytes, M0 macrophages, resting dendritic cells (DCs), and interleukin-10 (IL-10) were concentrated in the cluster A group. Additionally, based on the important WGCNA modules, we identified 7 key genes. Next, 240 samples were retyped based on 7 key genes; we found that T cells CD8, T cells CD4 memory activated, T cells follicular helper, and macrophages M1 were significantly increased in gene cluster-1. Finally, we performed functional enrichment of gene cluster-typed samples, showing potential functional differences between different types. Conclusions:Our study provides a review of the m6A regulators' expression pattern and functional importance in human AVC. The data from this study might serve as a significant resource for future mechanistic and therapeutic investigations into the role of critical m6A regulators in AVC.

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Distribution of Polymorphisms of the Renin—Angiotensin System Genes (ACE, AGT, and AGTR1), ITGB3, and FTO in Pregnant Patients with Hypertensive Disorders

Cited by 7 publications

References 8 publications

The critical roles of m6A modification in metabolic abnormality and cardiovascular diseases

The critical roles of m6A modification in metabolic abnormality and cardiovascular diseases

Association polymorphism of guanine nucleotide–binding protein β3 subunit (GNB3) C825T and insertion/deletion of the angiotensin-converting enzyme (ACE) gene with peripartum cardiomyopathy

Modification of m6A mediates tissue immune microenvironment in calcific aortic valve disease

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